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. Author manuscript; available in PMC: 2011 Jul 1.
Published in final edited form as: Arthritis Rheum. 2010 Jul;62(7):2004–2012. doi: 10.1002/art.27475

Figure 5.

Figure 5

TLR2/TLR4- and MyD88-dependent pro-catabolic responses to endogenously produced HMGB1. Immature mouse chondrocytes isolated from MyD88−/−, TLR2/TLR4−/−, TLR2−/−, TLR4−/− and congenic WT mice were transfected with HMGB1 cDNA, with an empty vector plasmid DNA used as a control. Forty-eight hours after transfection, the cells were placed onto poly-HEME coated plates. After three more days, release of HMGB1 was confirmed form the conditioned media by Western blot analysis (A). The conditioned media were analyzed for release of NO (B), MMP-3 and MMP-13 (C). Data for NO release from chondrocytes (n=3), and for MMP-3 and MMP-13 release from chondrocytes were representative of 3 individual experiments. Statistics for NO release in B, *, **p<0.005 for HMGB1 transfected MyD88−/− and TLR2/TLR4−/− relative to WT chondrocytes, respectively. Statistics for NO release in D, #p< 0.01 and ## p<0.04 for HMGB1 transfected TLR2−/− and TLR4−/− relative to WT chondrocytes, respectively.